OBJECTIVE -We performed a randomized trial to compare three insulin-titration protocols for tight glycemic control (TGC) in a surgical intensive care unit: an absolute glucose (Matias) protocol, a relative glucose change (Bath) protocol, and an enhanced model predictive control (eMPC) algorithm. RESEARCH DESIGN AND METHODS-A total of 120 consecutive patients after cardiac surgery were randomly assigned to the three protocols with a target glycemia range from 4.4 to 6.1 mmol/l. Intravenous insulin was administered continuously or in combination with insulin boluses (Matias protocol). Blood glucose was measured in 1-to 4-h intervals as requested by the protocols.RESULTS -The eMPC algorithm gave the best performance as assessed by time to target (8.8 Ϯ 2.2 vs. 10.9 Ϯ 1.0 vs. 12.3 Ϯ 1.9 h; eMPC vs. Matias vs. Bath, respectively; P Ͻ 0.05), average blood glucose after reaching the target (5.2 Ϯ 0.1 vs. 6.2 Ϯ 0.1 vs. 5.8 Ϯ 0.1 mmol/l; P Ͻ 0.01), time in target (62.8 Ϯ 4.4 vs. 48.4 Ϯ 3.28 vs. 55.5 Ϯ 3.2%; P Ͻ 0.05), time in hyperglycemia Ͼ8.3 mmol/l (1.3 Ϯ 1.2 vs. 12.8 Ϯ 2.2 vs. 6.5 Ϯ 2.0%; P Ͻ 0.05), and sampling interval (2.3 Ϯ 0.1 vs. 2.1 Ϯ 0.1 vs. 1.8 Ϯ 0.1 h; P Ͻ 0.05). However, time in hypoglycemia risk range (2.9 -4.3 mmol/l) in the eMPC group was the longest (22.2 Ϯ 1.9 vs. 10.9 Ϯ 1.5 vs. 13.1 Ϯ 1.6; P Ͻ 0.05). No severe hypoglycemic episode (Ͻ2.3 mmol/l) occurred in the eMPC group compared with one in the Matias group and two in the Bath group.CONCLUSIONS -The eMPC algorithm provided the best TGC without increasing the risk of severe hypoglycemia while requiring the fewest glucose measurements. Overall, all protocols were safe and effective in the maintenance of TGC in cardiac surgery patients. Diabetes Care 32:757-761, 2009

Recent studies focused on epicardial fat, formerly relatively neglected component of the heart, have elucidated some of its key roles. It possesses several properties that can distinguish it from other adipose tissue depots. Its unique anatomical location in the heart predisposes the epicardial fat to be an important player in the physiological and biochemical regulation of cardiac homeostasis. Obesity is associated with an increase in epicardial fat mass. Excess of cardiac fat can contribute to greater left ventricular mass and work, diastolic dysfunction and attenuated septal wall thickening. Imbalance in adipokines levels secreted in autocrine or paracrine fashion by epicardial fat can contribute to the activation of the key atherogenic pathways in the setting of metabolic syndrome. Epicardial fat has also been identified as an important source of pro-inflammatory mediators worsening endothelial dysfunction, eventually leading to coronary artery disease. Increased production of pro-inflammatory factors by epicardial fat can also contribute to systemic insulin resistance in patients undergoing cardiac surgery. Here we review the most important roles of epicardial fat with respect to heart disease in the context of other underlying pathologies such as obesity and type 2 diabetes mellitus.

Perioperative initiation of intensive insulin therapy during cardiac surgery reduces postoperative morbidity in nondiabetic patients while having a minimal effect in diabetic subjects.

Congestive heart failure represents a severe health condition with unfavourable long-term prognosis despite all the progress in pharmacological therapy of heart failure. Another therapeutic option is represented by mechanical cardiac support devices. Ventricular assist devices (VAD) constitute largest subgroup of these devices. Patients supported with VAD carry many considerations which are important for successful perioperative management of these patients for noncardiac surgery. The general perioperative considerations include consultation with VAD management personnel, detailed assessment of end-organ dysfunction before surgery, appropriate antibiotic prophylaxis, deactivation of implantable cardioverter-defibrillator for the time of surgical procedure, and the choice between general and regional anesthesia. Intraoperative monitoring depends primarily on the type of blood flow generated by VAD. For devices generating pulsatile blood flow, standard monitoring arrangements are needed. In the patients supported by devices which provide nonpulsatile blood flow, pulse oximetry and noninvasive blood pressure measurement are not reliable monitoring methods, and placement of intra-arterial catheter is warranted. In all the patients supported with VAD, transesophageal echocardiography is extremely useful method for monitoring the function of VAD itself, and in the case of univentricular VAD for monitoring the function of nonsupported cardiac ventricle. The most important issue in hemodynamic management of the patients with VAD is avoiding hypovolemia because it can cause inadequate VAD output with resulting low cardiac output and hypotension. All the patients with VAD need some degree of anticoagulation, and for noncardiac surgery the question of interrupting or decreasing the level of anticoagulation should be discussed among members of the caring team.

Dendritic cells (DCs) are professional antigen-presenting cells contributing to regulation of lymphocyte immune response. DCs are divided into two subtypes: CD11c-positive conventional or myeloid (cDCs) and CD123-positive plasmacytoid (pDCs) DCs. The aim of the study was to assess DCs (HLA-DR+ lineage-) and their subtypes by flow cytometry in peripheral blood and subcutaneous (SAT) and epicardial (EAT) adipose tissue in subjects with (T2DM, n=12) and without (non-T2DM, n=17) type 2 diabetes mellitus undergoing elective cardiac surgery. Subjects with T2DM had higher fasting glycemia (8.6±0.7 vs. 5.8±0.2 mmol/l, p<0.001) and glycated hemoglobin (52.0±3.4 vs. 36.9±1.0 mmol/mol, p<0.001) and tended to have more pronounced inflammation (hsCRP: 9.8±3.1 vs. 5.1±1.9 mg/ml, p=0.177) compared with subjects without T2DM. T2DM was associated with reduced total DCs in SAT (1.57±0.65 vs. 4.45±1.56% for T2DM vs. non-T2DM, p=0.041) with a similar, albeit insignificant, trend in EAT (0.996±0.33 vs. 2.46±0.78% for T2DM vs. non-T2DM, p=0.171). When analyzing DC subsets, no difference in cDCs was seen between any of the studied groups or adipose tissue pools. In contrast, pDCs were increased in both SAT (13.5±2.0 vs. 4.6±1.9% of DC cells, p=0.005) and EAT (29.1±8.7 vs. 8.4±2.4% of DC, p=0.045) of T2DM relative to non-T2DM subjects as well as in EAT of the T2DM group compared with corresponding SAT (29.1±8.7 vs. 13.5±2.0% of DC, p=0.020). Neither obesity nor coronary artery disease (CAD) significantly influenced the number of total, cDC, or pDC in SAT or EAT according to multiple regression analysis. In summary, T2DM decreased the amount of total dendritic cells in subcutaneous adipose tissue and increased plasmacytoid dendritic cells in subcutaneous and even more in epicardial adipose tissue. These findings suggest a potential role of pDCs in the development of T2DM-associated adipose tissue low-grade inflammation.